Equis ISSN 2398-2977

Keratitis: bacterial

Contributor(s): Dennis E Brooks, Alison Clode, Paul Gerding, Graham Munroe

Introduction

  • Cause: commensal external eye bacteria (often gram-negative) invade the stroma opportunistically following epithelial injury and/or long-term antibacterial/corticosteroid treatment.
  • Signs: should be suspected in horses with painful eyes where there is a sudden worsening and change in nature of ocular discharge; ocular pain and discharge, corneal edema and vascularization with ulceration (fluorescein positive); some cases develop keratomalacia as a serious complication.
  • Diagnosis: corneal scrapings/swabs for cytology (Diff-Quik, Wright-Giemsa or Gram stain) and culture - useful in choosing appropriate antibacterial therapy.
  • Treatment: medical therapy includes intensive topical antibacterial, mydriatic/cycloplegic and anti-ulcer medication; and systemic NSAIDs; surgical treatments may be necessary in resistant or severe cases.
  • Prognosis: guarded and substantially worsened in cases of keratomalacia.

Pathogenesis

Etiology

  • Normal microflora of external eye are principally gram-positive organisms   Eye: microbiology - overview  .
  • Organisms frequently isolated in bacterial keratitis are usually gram-negative organisms, eg:
  • Occasionally gram-positive organisms are isolated:
  • Mixed bacterial (gram-negative) and fungal infections (Aspergillusspp   Aspergillus spp  ) are associated with severe corneal ulcers   Keratitis: mycotic  .
  • Factors known to determine keratopathogenicity:
    • Localization of bacteria to external eye may occur through long-term or incorrect topical antibiotic treatment distorting the resident commensal flora.
    • Exposure of corneal adherence receptor sites (on basal epithelium or anterior stroma), often following trauma.
    • Corneal penetration and dissemination ability of organism.
    • Previous therapy with topical steroids may inhibit healing of ulcer and increase susceptibility to infection, both bacterial and fungal.
  • Speed and intensity of ulcer formation will depend upon the bacterial keratophathogenicity and the efficacy of innate antiprotease mechanisms of the external eye (in tears and the cornea) in modulating the rate of corneal enzyme associated lysis.

Predisposing factors

General
  • Previous corneal epithelial damage.
  • Deficient inherent antimicrobial defence mechanisms, eg abnormalities of tear production, KCS.

Specific

  • Long-term topical ocular antibiotic treatment.
  • Long-term topical ocluar corticosteroid treatment.
  • Collagenolytic enzymatic degradation of cornea.

Pathophysiology

  • Bacteria are rarely able to damage or penetrate healthy corneal epithelium. The horse cornea is approximately 0.8-0.9 mm thick.
  • Once the epithelial barrier is damaged, often by trauma   Keratitis: traumatic / ulcerative  , the bacteria are able to adhere, penetrate and establish an infection in the stroma.
  • A wide range of bacteria is found in the normal eye, and these populations are subject to marked seasonal and geographical variation   Eye: microbiology - overview  .
  • Most bacteria involved in infections are opportunistic, gram-negative, commensals - some of which apppear to possess specific keratopathogenic proteases.
  • The intensity of the host response to corneal injury and/or infection, in some horses, results in extensive and rapidly progressing deep stromal necrosis and ulceration (stromal liquefaction or 'melting') which can be eye-threatening.
  • Following epithelial injury, microbial colonization of the cornea may occur inciting a host response characterized by inflammatory cell invasion and vascularization.
  • In many cases this host response is effective in resolving the infection and corneal healing proceeds to its conclusion.
  • In some cases, because of specific keratopathogenic factors, the infection becomes established and increases corneal damage through bacterial and inflammatory cell (PMNs and macrophages) toxins and proteases, resulting in cell death.
  • Severe keratomalacia or stromal 'melting' occurs through massive collagenolysis, which may result in corneal perforation and iris prolapse.
  • The most well known organism capable of producing collagenolytic enzymes isPseudomonas aeruginosa  Pseudomonas aeruginosa  , but beta-hemolyticSteptococcusspp   Streptococcus spp  also produce powerful proteases.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Hamor R Eet al(1999)Equine infectious keratitis.Vet Clin North Am Equine Pract15(3), 623-646, ixPubMed.
  • Nasisse M P & Nelms S (1992)Equine ulcerative keratitis.Vet Clin North Am Equine Pract8(3), 537-555PubMed.

Other sources of information

  • Andrew S E & Willis A M (2005)diseases of the Cornea and Sclera.In:Equine Ophthalmology.Ed: Gilger B C. Elsevier Saunders. pp 157-251.
  • Barnett K C, Crispin S M, Lavach J D & Matthews A G (2004)Equine Ophthalmology - An Atlas and Text.2nd edn. W B Saunders.
  • Brooks D E (1999)Equine Ophthalmology.In:Veterinary Ophthalmology.Ed: Gelatt K N. 3rd edn. pp 1053-1116.


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